It is known that appreciable levels of AChE are present in ocular tissues such as the amacrine cells of the retina (Hutchins, H. B. and Hollyfield, M. G. (1987) "Acetylcholinesterase in the human retina" Brain Res. 00, 300-311), and the nerve plexuses of the iris (Mattio, T. G. et al, (1984) "Effects of DFP on iridic metabolism and release of acetylcholine and on pupillary function in the rat" Neuropharmacology, 23, 1207-1214). It would therefore be expected that any secretion of AChE from such tissues would result in detectable levels of enzymatic activity within the fluids of the eye. Although there are some reports from the 1940s of cholinesterase activity in ocular fluids of various mammalian species (De Roeth, A., (1950) "Cholinesterase activity in ocular tissues and fluids," Arch. Ophthalmol. 43, 1004-1025) no attempt was made to distinguish between AChE and butyrylcholinesterase (BuChE) activities. Furthermore, these reports have not been confirmed by modern assay methods.
Patients with senile dementia of the Alzheimer-type (SDAT) frequently have defects in visual perception and find difficulties in performing visual tasks. Histological and electrophysiological studies indicate that these defects may be due to degenerative changes at all levels of the visual pathways, including loss of retinal ganglion cells and axonal degeneration of the optic nerve. The lower levels of acetylcholinesterase (AChE) observed in the post-mortem brains of patients with SDAT as a result of neuronal degeneration are reflected by lower levels of AChE in ventricular cerebrospinal fluid (CSF) obtained at post-mortem (Appleyard, M. E., et al (1987) Brain 110, 1309-1322).
Inasmuch as it is well established that AChE is present in ocular tissue including in the inner plexiform layer of human retina, if there are differences in the AChE content of fluids from patients with histologically diagnosed SDAT and normal aged-matched controls, these differences could be employed in diagnosing the presence or absence of SDAT.